New Therapeutics for Traumatic Brain Injury Prevention of Secondary Brain Damage and Enhancement of Repair and Regeneration (2017) (PDF) Kim Heidenreich

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New Therapeutics for Traumatic Brain Injury Prevention of Secondary Brain Damage and Enhancement of Repair and Regeneration (2017) (PDF) Kim Heidenreich

Basic Information:

  • Year: 2017
  • Page Number: 317
  • File Type: PDF
  • File Size: 9.18 MB
  • Authors/ Editiors: Kim Heidenreich

Description:

New Therapeutics for Traumatic Brain Injury: Prevention of Secondary Brain Damage and Enhancement of Repair and Regeneration explores traumatic brain injury (TBI), a major cause of death and disability throughout the world. The delayed nature of the secondary injury phase suggests that there is a therapeutic window for pharmacological interventions or other approaches to prevent progressive tissue damage and improve functional outcomes. It is now apparent that therapeutic interventions should entail both protective and repair/regeneration strategies depending on the phase of brain injury.

This book describes emerging experimental strategies for the treatment of TBI, including new anti-inflammatory or anti-apoptotic therapeutics that limit brain damage, and novel or repurposed drugs that enhance repair or regeneration of the brain after injury.

Kim A. Heidenreich is Professor of Pharmacology and Neuroscience at the University of Colorado School of Medicine. She also serves on the Keystone Scientific Advisory Board and is Chief Scientific Advisor for the American Traumatic Brain Injury Association. Dr. Heidenreich has been conducting neuroscience research for over 30 years with continual funding in the area of neurotrophic factors, mechanisms of neuronal cell death, and recently, traumatic brain injury (TBI). Her laboratory has identified a number of protein kinase signaling pathways that trigger or prevent neuronal cell death in response to neuronal insults and neurotrophic factors, respectively. She has examined the ways in which key proapoptotic and antiapoptotic protein kinases regulate cytoplasmic, mitochondrial, and nuclear targets to control neuronal apoptosis and autophagy. Her recent studies have focused on preventing secondary brain damage after a TBI. She has recently discovered that leukotrienes, potent inflammatory lipid mediators normally absent in brain, are produced by a transcellular mechanism involving infiltrating neutrophils after TBI. Blockade of leukotriene production using 5-lipoxgenase (FLAP) inhibitors prevents edema, cell death, and cognitive deficits after TBI. These findings have important implications for treating human TBI and suggest that development of FLAP inhibitors for use in TBI is feasible for both intervention and prevention. Toward this goal, Dr. Heidenreich is currently developing FLAP inhibitors with improved CNS properties and novel delivery methods for these drugs in TBI.

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